The fast carbs will give you a insulin spike.
A professor on sports medicine told me that there has been shown no difference, going as low as 6 grams of amino acids post workout.
It's all about the carbs, those will give a insulin release. A sports scientist told me that 180 grams of carbs post workout would be something to try to get a kickass insulin release. And he also told me to keep the protein low, as that will slow down the carbs.
YIP
Zack
Yes, but the insulin spike will do you no good in the long run.
The carbs are absorbed anyway, so low GI carbs will do. As for the protein, i don't take protein shakes at all.
5-8g BCAA after a workout followed by 20g amino acids 30 minutes later followed by a whole meal 30 minutes later.
The insulin spike every time you work out kills your insulin sensitivity, which means you will need more and more carbs to spike your insulin.
i take 4-6 g of cinnamon each day to keep insulin sensitivity high, then low carbs or very little carbs will do.
Studies show that cinnamon supplementation helps with insulin sensitivity.
Study given below.
Bioactive compounds extracted from cinnamon potentiate insulin activity, as measured by glucose oxidation in the rat epididymal fat cell assay. Wortmannin, a potent PI 3'-kinase inhibitor, decreases the biological response to insulin and bioactive compounds from cinnamon similarly, indicating that cinnamon is affecting an elements upstream of PI 3'-kinase. Enzyme studies done in vitro show that the bioactive compounds can stimulate autophosphorylation of a truncated form of the insulin receptor and can inhibit PTP-1, a rat homolog of a tyrosine phosphatase (PTP-1B) that inactivates the insulin receptor. No inhibition was found with alkaline phosphate or calcineurin suggesting that the active material is not a general phosphatase inhibitor. It is suggested, then, that a cinnamon compounds, like insulin, affects protein phosphorylation-dephosphorylation reactions in the intact adipocyte. Bioactive cinnamon compounds may find further use in studies of insulin resistance in adult-onset diabetes.
Cinnamon Improves Glucose and Lipids of People With Type 2 Diabetes
Alam Khan, MS, PHD1,2,3, Mahpara Safdar, MS1,2, Mohammad Muzaffar Ali Khan, MS, PHD1,2, Khan Nawaz Khattak, MS1,2 and Richard A. Anderson, PHD3
1 Department of Human Nutrition, NWFP Agricultural University, Peshawar, Pakistan
2 Post Graduate Medical Institute, Hayatabad Medical Complex, Peshawar, Pakistan
3 Nutrients Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, Beltsville, Maryland
Address correspondence and reprint requests to Dr. Richard A. Anderson, Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, Bldg. 307, Rm. 224, Beltsville, MD 20705. E-mail: Anderson@307.bhnrc.usda.gov
OBJECTIVE—The objective of this study was to determine whether cinnamon improves blood glucose, triglyceride, total cholesterol, HDL cholesterol, and LDL cholesterol levels in people with type 2 diabetes.
RESEARCH DESIGN AND METHODS—A total of 60 people with type 2 diabetes, 30 men and 30 women aged 52.2 ± 6.32 years, were divided randomly into six groups. Groups 1, 2, and 3 consumed 1, 3, or 6 g of cinnamon daily, respectively, and groups 4, 5, and 6 were given placebo capsules corresponding to the number of capsules consumed for the three levels of cinnamon. The cinnamon was consumed for 40 days followed by a 20-day washout period.
RESULTS—After 40 days, all three levels of cinnamon reduced the mean fasting serum glucose (18–29%), triglyceride (23–30%), LDL cholesterol (7–27%), and total cholesterol (12–26%) levels; no significant changes were noted in the placebo groups. Changes in HDL cholesterol were not significant.
CONCLUSIONS—The results of this study demonstrate that intake of 1, 3, or 6 g of cinnamon per day reduces serum glucose, triglyceride, LDL cholesterol, and total cholesterol in people with type 2 diabetes and suggest that the inclusion of cinnamon in the diet of people with type 2 diabetes will reduce risk factors associated with diabetes and cardiovascular diseases.
Cinnamon Extract Prevents the Insulin Resistance Induced by a High-fructose Diet
B. Qin 1, M. Nagasaki 2, M. Ren 3, G. Bajotto 1, Y. Oshida 1, 2, Y. Sato 1, 2
1 Department of Sports Medicine, Graduate School of Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
2 Research Center of Health, Physical Fitness and Sports, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
3 Department of Visual Neuroscience, Graduate School of Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan
Abstract
The aim of this study was to determine whether cinnamon extract (CE) would improve the glucose utilization in normal male Wistar rats fed a high-fructose diet (HFD) for three weeks with or without CE added to the drinking water (300 mg/kg/day). In vivo glucose utilization was measured by the euglycemic clamp technique. Further analyses on the possible changes in insulin signaling occurring in skeletal muscle were performed afterwards by Western blotting. At 3 mU/kg/min insulin infusions, the decreased glucose infusion rate (GIR) in HFD-fed rats (60 % of controls, p < 0.01) was improved by CE administration to the same level of controls (normal chow diet) and the improving effect of CE on the GIR of HFD-fed rats was blocked by approximately 50 % by N-monometyl-L-arginine. The same tendency was found during the 30 mU/kg/min insulin infusions. There were no differences in skeletal muscle insulin receptor (IR)-β, IR substrate (IRS)-1, or phosphatidylinositol (PI) 3-kinase protein content in any groups. However, the muscular insulin-stimulated IR-β and IRS-1 tyrosine phosphorylation levels and IRS-1 associated with PI 3-kinase in HFD-fed rats were only 70 ± 9 %, 76 ± 5 %, and 72 ± 6 % of controls (p < 0.05), respectively, and these decreases were significantly improved by CE treatment. These results suggest that early CE administration to HFD-fed rats would prevent the development of insulin resistance at least in part by enhancing insulin signaling and possibly via the NO pathway in skeletal muscle.
